Stromal cell-derived factor 1 promoted migration of adipose-derived stem cells to the wounded area in traumatic rats.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Adipose-derived stem cells (ADSCs) were effective in treating wound. Stromal cell-derived factor-1 (SDF-1), a chemokine usually called CXCL12, is well known for its chemotaxis in induction of cell migration. However, little is known about the SDF-1responsible for the complex migration of ADSCs from residence to injured sites. Objective Herein, we firstly showed SDF-1 is a major regulator involved in migration of ADSCs during wound repair in vivo. Methods Trauma in rats was induced by surgical operation. The levels of SDF-1 in wounded tissue were assayed by ELISA. ADSCs were labeled with Green Fluorescent Protein (GFP), and then were transferred to injured rats by intracarotid injection. The plasma levels of ADSCs during wound healing were detected by flow cytometry, and ADSCs in injured tissue were evaluated by bioluminescence imaging in vivo and laser confocal microscopy (LCM), respectively. Results ADSCs were successfully labeled with GFP. SDF-1 level reached to the peak value on 24 h after injury and then decreased continuously. Additionally, levels of plasma ADSCs in SDF-1 treated rats reached to the peak value (12%) at d21 after medicine delivery, while those of normal and injured rats showed the peak values of 6.28% and 9.84% at d7 and d21, respectively. Finally, the results of LCM indicated treatment of ectogenic SDF-1 obviously enhanced GFP-ADSCs distribution

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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